Posner B I
Endocrinology. 1976 Mar;98(3):645-54. doi: 10.1210/endo-98-3-645.
The specific binding of 125I-labeled insulin, human hormone ([125I]hGH), bovine growth hormone ([125I]bGH), and ovine prolactin ([125I]oPRL) was studied in mouse liver membranes. [125I]hGH and [125I]oPRL bound to adult liver membranes. Pregnancy increased the specific binding of [125I]hGH but not that of [125I]oPRL. [125I]hGH was displaced from membranes of pregnant mice by hGH, oPRL, and bGH, but only by hGH and oPRL from liver membranes of nonpregnant mice. Significant specific binding of [125I]bGH was seen only in pregnancy. The binding of [125I]bGH to pregnant mouse liver membranes increased with increasing concentration of either membrane protein or [125I]bGH. Both the specific binding and dissociation of [125I]bGH were greatly influenced by the time and temperature of incubation. Binding of [125I]bGH was inhibited by growth hormones, including hGH and rat GH, and not by lactogenic hormones (various prolactins and human placental lactogen), ACTH, glucagon, or insulin. The inhibition of [125I]hGH binding by hGH and bGH, in the presence of excess (2 mug/ml) of PRL, was very similar to that seen with [125I]bGH. Scatchard plots of displacement dose-response curves obtained under steady state conditions of 4C were nonlinear and very similar with either [125I]bGH or [125I]hGH. This contrasted with the linear Scatchard plots obtained from displacement dose-response curves of either [125I]oPRL or [125I]hGH in the presence of excess (2 mug/ml) bGH. Termination of pregnancy, either naturally or by hysterectomy, reduced [125I]bGH specific binding to nonpregnant levels by 24 to 36 h. Estrogen administration did not increase [125I]bGH binding in hepatic membranes. Nonpregnant mice possess hepatic lactogen binding sites which are uninfluenced by pregnancy. GH specific binding sites are markedly augmented during pregnancy. The close correlation between the level of these sites and pregnancy suggests that they are regulated by a product of the fetoplacental unit.
在小鼠肝细胞膜中研究了125I标记的胰岛素、人激素（[125I]hGH）、牛生长激素（[125I]bGH）和羊催乳素（[125I]oPRL）的特异性结合。[125I]hGH和[125I]oPRL与成年肝细胞膜结合。怀孕增加了[125I]hGH的特异性结合，但未增加[125I]oPRL的特异性结合。hGH、oPRL和bGH可使[125I]hGH从怀孕小鼠的膜上解离，但只有hGH和oPRL可使[125I]hGH从未怀孕小鼠的肝细胞膜上解离。仅在怀孕时可见[125I]bGH有显著的特异性结合。[125I]bGH与怀孕小鼠肝细胞膜的结合随膜蛋白或[125I]bGH浓度的增加而增加。[125I]bGH的特异性结合和解离均受孵育时间和温度的极大影响。[125I]bGH的结合受到包括hGH和大鼠GH在内的生长激素的抑制，而不受催乳激素（各种催乳素和人胎盘催乳素）、促肾上腺皮质激素、胰高血糖素或胰岛素的抑制。在存在过量（2μg/ml）PRL的情况下，hGH和bGH对[125I]hGH结合的抑制作用与[125I]bGH的情况非常相似。在4℃稳态条件下获得的置换剂量反应曲线的Scatchard图是非线性的，并且[125I]bGH或[125I]hGH的情况非常相似。这与在存在过量（2μg/ml）bGH的情况下从[125I]oPRL或[125I]hGH的置换剂量反应曲线获得的线性Scatchard图形成对比。自然分娩或子宫切除终止妊娠后，24至36小时内[125I]bGH的特异性结合降至未怀孕水平。给予雌激素并未增加肝细胞膜中[125I]bGH的结合。未怀孕小鼠具有不受怀孕影响的肝催乳素结合位点。怀孕期间GH特异性结合位点明显增加。这些位点的水平与怀孕之间的密切相关性表明它们受胎儿胎盘单位产物的调节。
